By\King of pathology( Legand Hazem )

A-Inflammation
Def.: It is a local response of living tissue to injurious agent w` consists of a series
of vascular, lymphatic & local tissue changes.
The suffix itis is usually added to organs name to designate its inflammatory nature as tonsillitis &
appendicitis.
AIM OF INFLAMMAION:
1. destroy, dilute, remove or localie injurious agents.
!. prepare tissue for repair.
FAIL!"# OF INFLAMMAO"$ "#A%ION L#AD& O
1. spread of infection .
!. no healing of "urns & wounds.
%A!&#& OF INFLAMMAION: # injurious agents w cause inflammation are called irritants,
These may "e:
$%& 'iving irritants: "acteria, viruses, fungi & parasites .
$(& )on living irritants: Include :*
*+hysical irritants: %s mechanical trauma, heat, cold, electricity, ioniing radiation.
*,hemical irritants as acids, al-alis.
*)ecrotic tissue : Irritate adjacent living tissue.
*Immune mechanism $%g I %" reaction&
BAL#'"O!ND: the defense forces of the "ody meat the irritant in the ground su"stance of ,T
.
$(#& OF INFLAMMAION: %ccording to the d)*ation of irritation, it is classified into:-
A+)te inflammation %h*oni+ inflammation
I**itant .evere. /ild.
On,et .udden. 0radual.
D)*ation .hort 1 days 2 wee-s 3. 'ong 1 months 2 years 3.
-a,+)la*
+hnge,
/ar-ed. /ild.
Bl. -e,,el Thin 2 dilated 2 congested. Thic- 1 4%5 3.
Inflam. +ell, /acrophage * neutrophil * pus cell. /acrophage 2lymphocyte 2 pl. cell 2
giant cells.
A**angment 6iffuse. +erivascular or diffuse.
Ma+*ophage 7rom "lood monocytes. 7rom tissue histocutes.
"/. 4xudative. +roliferative.
Fi0*o,i, %"sent or mild. /ar-ed.
"epai* 7ollow. %ssociate.
o/emia .evere. /ild.
%a*dinal
&ign,
8ed 2 hot 2 pain 2 swelling 2 loss of
function.
)ot present except swelling.
'ene*al
+hange,
7ever present.
'eucocytosis present.
%"sent.
)ormal or
ype, .uppurative or non suppurative. .pecific or non specific.

Acute inflammatory cells Chronic inflammatory cells
- Netro!"ils#
- $acro!"a%e#
- &aso!"ils#
- 'osino!"ils#
- ()*!"oc)tes#
- $acro!"a%e#
- +las*a cells#
- ,iant cells , fi-roc)tes#
A%!# INFLAMMAION
1\ 'ene*al +h2 of a+)te inflammation :*
.udden onset.
.hort duration.
.evere irritant.
.evere tissue injury.
3\ Mo*phologi+al +hange, in a+)te inflammation45
1)-A&%!LA" %HAN'#& (-A&%!LA" (H#NOM#NON).
3)#6!DAI-# %HAN'#&.
7)LO%AL I&&!# %HAN'#&.
1& -A&%!LA" %HAN'#&( LO%AL -A&%!LA" (H#NOM#NON&
%nti"odies & 9(,s $defense mechanisms& are carried in "lood hence the importance of vascular
changes in acute inflammation:*
1* Transient :., : due to direct effect of irritant on "l. vessel.
!* +ermanent :.6 : due to chemical mediators.
;* (lood flow: hydrostatic pressure hotness , redness.
<* 7luid exudates : escape of plasma rich in proteins to interstitial tissue through high
permea"ility of capillaries.
=* .lowing of "lood flow due to :*
a& Increase viscosity due to fluid exudates.
"& 5pening of capillary "ed.
c& .welling of endothelial cells project into lumen resist "lood flow.
85 %ell)la* e/)date, 4 9 +hange in 0lood +ell, 45
:Def. : 4scape of some leucocytes outside "lood vessel towards irritant guided "y chemotactic
agents.
:&tep, 9 me+hani,m :
1. /igration of leucocytes # pavementation of endothelium :*
'eucocytes leave axial stream stea- to endothelial cells first loosly then "ecome
adherent due to slowing of "l.flow & chemical mediator.
!. 4migration of leucocytes : active process
9(,s move "y amoe"oid movement through inter*endothelial gaps towards irritant.
;. 6iapedesis of 8(,s : passive process
.ome 8(,s pushed "y "lood pressure & follow passage of leucocytes
<. ,hemotaxis : directional amoe"oid movement of leucocytes on fi"rin threads towards
irritant guided "y chemotactic agent.
=. +hagocytosis : 1 discussed after 3 .
Be,t ;i,he,
!& #6!DAI-# (H#NOM#NON (%HAN'#&&
vascular changes escape of plasma 9(,s from "lood vessels into the interstitial tissue forming >
inflammatory exudate w` consists of.
$%&fluid component $fluid exudate&
$(&cellular component $cellular exudate&
A5Fl)id e/)date,
Def. : accumulation of plasma fluid rich in protein in imterstitial spaces due to acute
inflammation process.
(athogene,i, 9 aetiology 4
1. increase hydrostatic pressure : increase "lood flow.
!. increase capillary permea"ility due to damage of endothelium& widening of inter*
endothelial spaces.
;. increase tissue osmotic pressure due to escape of pl.protein into interstitial spaces.
<. .plitting of large molecules of pl.protein into small ones.
Amo)nt : depend on :
- nature of irritant : excess in toxins.
- .ite of inflammation : excess in loose area ? scanty in solid area.
- .tate of lymphatics : decrease drainage of fluid exudates its accumulation.
%ompo,ition : contain protein 2 fi"rin 2 inflammatory cells.
Fl)id e/)date, Fl)id t*an,)date
Def. %s "efore. )ormal fluid present in tissue "ut when
increase : cause edema
Aetiology %s "efore. Increase capillary pressure.
Fo*mation %ctive. +assive.
(tn +ontent < * @ gmA B < gmA
Inflam.+ell, +resent. %"sent.
Fi0*in
+ontent
8ich in fi"rin , so clot on standing. 'ittle , so not clot on standing.
&pe+ifi+
g*a<ity
C 1D1@ B 1D1<
F!N%ION:
*%& 6iluting > irritant specially chemical & "acterial toxins.
*(& It "rings anti"odies to > site of inflammation.
*c& Eigh fi"rinogen content formation of > fi"rin w serves as:30=3p
i* Ba**ie* preventing spread of "acteria.
ii* %ct as 0*idge for inflam. cells & repair cells.
iii* .urface phago+yto,i,.
iv*formation of fi0*in pl)g, that o"struct lumphatics to prevent lymphatic spread of infection.
d& ,arries away waste products of ,s & supplies their nutrition.
Be,t ;i,he,
B5%ell)la* e/)date
The 9(,s escape outside the circulation "y:
$1& /argination $mentioned& $!& 4migration $mentioned&
$;& ,hemotaxis. $<& +hagocytosis.
%H#MOA6I& :
:Def 4 directional movement of 9(,s towardsthe irritant e` in the area of acute inflammation.
:+hemota+ti+ agent,:
1*exogenous : "acterial products
!* endogenous :* ,omplement system
:Me+hani,m of a+tion:*
,hemotactic agents "ind to receptors on 9(,s FF intracellular contractile proteins
leu-ocyte movement.
:%ha*a+te*, : specific : each organism attract specific leucocytes :*
- cocci attract neutrophils.
- (acilli attract monocytes.
- +arasite attract eosinophils.
(HA'O$O&I&4
a5Def # process "y w neutrophils $microphages&& macrophages ingest , destroy organisms,
necrotic de"ris & foreign particles
* phagocytic ,s are :$1& /acrophages.
$!&)eutrophils .
$;&7oreign "ody giant ,s.
05Me+hani,m of phago+yto,i,:
1. 8ecognition , attachment : * phagocytic cells attach firmly to irritant.
* in case of living irritant , attachment is helped "y :*
a. opsoniation : fixation of organism to %" to "e phagocytosed.
". .urface phagocytosis : fixation against fi"rin networ- or tissue surface.
!. Indigestion : when organism is attached to surface of leucocytes surface
pseudopodia emerge fuse together to engulf organism forming phagosome.
;. 6igestion : lysosome F phagosome phagolysosome discharge of
lysosomal content to -ill organism.
<. Gilling : "y * 5! dependent system "y 5! meta"olites , E! superoxide.
* 5! independent system "y lysosomal enyme.
1 chemotaxis & phagocytosis 3 . /0 1234 5 678 9:; <= >? @
D#F#%I-# (HA'O%$O&I&4
Def4 0roup of disease ch` "y defect in one or more steps of phagocytosis.
(A)#/t*in,i+(a+>)i*ed) defe+t, :
$1& .teroids
$!&)eutropenia
$;& .ystemic diseases as dia"etes, nephrotic syndrome & advanced
malignancy.
Be,t ;i,he,
(B)Int*in,i+ defe+t, (+ongenital)45
1* %h*oni+ g*an)lomato),
di,ea,e of +hildhood
!* %hedia?5 Higa,hi
,ynd*ome.
;* Lazy le)?o+yte
,ynd*ome
*.ex lin-ed recessive
*/icrophages & macrophages do
not meta"olie 5! canHt -ill
some microorganisms.
*%utosomal recessive
Itcomprises:
a*)eutropenia
"*6efective chemotaxis
c*)on destruction of
phagocytosed "acteria,
*It is fatal
defect in neutrophil
motility
;& LO%AL I&&!# %HAN'#&
'ocal tissue change 1 necrosis , degeneration 3 :*
* ,ells in center of inflame. %rea are necrosed & surrounding os degenerated.
* (oth cells release chemical mediator FFvascular phenomenon.
* 'ocal transformation of histiocytes to macrophage.
%A"DINAL &I'N& OF A%!# INFLAMMAION4
9Na?ed eye pi+t)*e(N@#)
$1&8edness:*> first sign noted in > inflamed area . It is d.t :.6 of capillaries.
$!& Eotness:* sign of inflammation of "ody $ & s-in. It is d.t :.6 FF& "l. 7low.
$;&.welling:* d.t FF "lood flow & accumulation of fluid exudate.
$<& +ain: d.t : chemical mediators.
$=&'oss of function : d.t : +ain & tissue destruction.
M@# of a+)te inflammation:
$1& 6ilatation of arterioles, venules & capillaries.
$!& 4dema : pale red homogenous material & separate tissue ,s.
$;& %cute inflammatory ,s : neutrophils, macrophages, some 8(,s.
$<& 7i"rin threads.
&y,temi+ effe+t, of a+)te inflammation 9 gene*al +hange,
$1)Fe<e* :* when infection associated e spread of> organisms into > "lood.
,ause : pyrogens $i.e. fever producing&
%& 4xogenous: released from "acteria & fungi.
(& 4ndogenous: from 9(,s as cyto-ines $specially interleu-in 1 # I'*1 & tumor
necrosis factor #T)7&. They FF heat regulating center of hypothalamus sympathetic nerve
stimulation & :.,. of s-in vessels, ** heat loss fever.
* 7ever destroy "acteria "ut also harmful to "ody
$3)Le)+o+yto,i,: ,ommon e "acterial infection.
,ause : FF 9(,s from "one marrow "y I'*I & T)7
).(: in typhoid leucopenia.
75 %hange in pla,ma p*otein le<el 4
increase secretion of protein "y liver as 1 fi"rinogen 2 ceruloplasmin 2
c reactive protein III3 : * increase 4.8.
A5 Othe*, : as tachycardia , hypertension , III
Be,t ;i,he,
%H#MI%AL M#DIAO"& OF A%!# INFLAMMAION
A5Def4 chemical su"stance control process of acute inflammation.
They include:*
$1& %ell)la* fa+to*,:
$%& %mines : histamine & serotonin are released from mast ,s, "asophils & platelets.
$(& +rostaglandins: released from most ,s.
$,& 'eu-otrienes: secreted "y neutrophils.
$6& lysosomal components: released from neutrophils, macrophages & platelets.
$!&(la,ma fa+to*,4
$%& Ginin system e.g. "rady-inin formed as follows
$(& ,omplement system: series of plasma proteins, present as inactive forms in
plasma $num"ered ,1 ,J&. %ctivation either "y:*
$1& ,lassical pathway: triggered "y fixation of ,1 to %g?%" complex
$!& %lternative pathway: triggered "y activation of ,; "y %g?%" complex or "y
certain "acterial endotoxin.
The main active products of complement system are ,;a & ,=a#anaphylatoxin
w` share in anaphylactic shoc-.
$,& ,oagulation system:* ,hanges fi"rinogen fi"rin.
$6& 7i"rinolytic system: 6issolves fi"rin.
B5Main a+tion, of +hemi+al mediato*, a*e49 F)n+tion, :
$1& :ascular dilatation: e.g. "y histamine.
$!&FF:ascular permea"ility : histamine & -inins
$;& ,hemotaxis: leu-otrienes , lysosomal components & ,=a
$<& +ain: "rady-inin.
$=& 7ever : I' ,+0s.
$K& 'eucocytosis : I' , T)7.
ype, of a+)te inflammation
I* .uppurative inflammation.
II* )on* .uppurative inflammation
I- Acute suppurative inflammation
Def: .evere acute inflammation characteried "y pus formation.
%a),e,: +yogenic $ pus forming& "acteria as staphylococcus aureus,
streptococcus hemolyticus, pneumococcus, gonococcus &4*coli.
(),: Is the fluid formed d.t liLuefaction of necrotic tissue & fi"rin "y proteolytic
enymes .
pathogene,i, of p), fo*mation4 Fo* ,)pp)*ation to o++)* 7 fa+to*, a*e *e>)i*ed4
1. Tissue necrosis : produced "y * powerful toxins of pyogenic "acteria.
* presence of inflammatory edema.
* throm"osis due to slowing of "l.flow & endothelial injury.
There is chemotaxis of large no of neutrophils.
!. .truggle occur $ & large no of neutrophil & "ateria death of neutrophils
transformed to pus cells.
;.+us cells produce proteolytic enyme liLuefy $necrotic tissue 2 organism 2
inflame.cells 1 dead, living 3 2 fi"rin w` "ecome mixed e` fluid exudates& forming +us.
%ompo,ition: * necrotic tissue 1 main participate 3
* organism * inflame. cells * fluid exudates
* in old pus : macrophage , cholesterol crystals , fat glo"ules are present.
%ha*a+te*, of p), of ,taphylo+o++), a)*e), :
1.Thic- tur"id & viscous d.t remnants of tissue destruction especially 6)%.
!.%l-aline pE.
;.Mellowish d.t myeloperoxidase of neutrophils.
<.5dorless.
=.6oes not clot on standing d.t destruction of fi"rinogen "y proteolytic enymes.
Types of suppurative inflammation 4
I*'ocalied: 1* %"scess. !*(oil $7uruncle& ;*,ar"uncle.
II*6iffuse: e.g. ,ellulitis, suppurative appendicitis... etc.
A0,+e,,
Def: % localied suppurative inflammation > formation of an irregular cavity
containing pus.
%a),e: staphylococcus aureus.
&ite: any where $,ommon sites are: s-in, lung, "rain, -idney, liver.... etc.&
(athogene,i, of a0,+e,, :
1. 1
,t
pathogenesis of pus 1 as "efore 3
!. 3
nd
: co*agulase enyme divide it into ones :*
early : * central necrotic tissue.
* peripheral area of acute inflame. surround it.
'ate : * central necrotic tissue.
* pus cavity surround it.
* area of acute inflammation 1 pyogeni+ mem0*ane 3 surround it e` excess
neutrophils.
N@# : cardinal signs of acute inflammation as "efore$ .&
Nones 1 early , late 3 as "efore.
M@# : /?4 of acute inflammation F acute inflammatory cells
1 mainly neutrophils, pus cells 3.
Fate of a0,+e,, : any pus in "ody must "e evacuated "ecause pus can`t "e a"sorped 1 3
* pus can "e evacuated either :
1. .urgical method : healing.
!. .pontaneously : complications w` are :
a. local : * ulcer : discontinuity of surface epithelium.
* sinus : "lind tract open on surface.
* fistula : tract connect ! surface epithelium.
* lymphadenitis : inflammation of '.)s
* lymphangitis : inflammation of lymph vessels.
* phele"itis : inflammation of veins.
". .ystemic : if spread:
* toxemia : toxins in "lood.
* pyaemia : circulation of septic em"oli in "lood e` localiation
* septicemia : circulation , multiplication of large )o of
pathogenic "acteria & their toxins in "lood e`out localiation.
c. ,hronicity : change to chronic a"scess:
)?4 : has thic- fi"rous wall , smooth lining , covered "y some pus w` may
"e calcified , surrounded "y mild hyperaemic ones.
/?4 : as chronic inflammation 1 discussed after 3.
A+)te a0,+e,, %h*oni+ a0,+e,,
&ame a, +ompa*i,on 0et;een a+)te B +h*oni+ inflam. ( ) 0)t
Linin
g
(),
8ough due to fi"rin.
Thin.
.mooth due to fi"rosis.
Thic-.
F)*)n+le (Boil)
Def: It is small a"scess related to hair follicle, se"aceous or sweat gland.
%a),e: staphylococci.
&ite: mainly hairy parts as face, axilla.
*/ultiple neigh"oring "oils are called furunculosis.
%a*0)n+le
Def. : .pecial type of a"scess ch` "y intercommunicating suppurative foci opening
on surface e` multiple sinuses.
%a),e 9 aetiology :
1. .taphylococci "ecause it is pyogenic & produce co*agulase enyme.
!. Thic- s-in.
;. 6./ 1 dia"etes mellitus 3 : common predisposing factor.
(athogene,i, 4
1. +athogenesis of pus ABC@
!. ,ollagen "undles formation.
N@# : 1. site : thic- s-in . 4x: "ac- of nec- ,
!. cardinal signs of acute inflammation : ABC@
;. multiple sinuses discharging pus.
M@# : %s a"scess ABC@
%ompli+ation: %s a"scess "ut more li-ely ABC@
Diff),e ,)pp)*ati<e inflammation9 %ell)liti, (phlegmono), inflammation)
%ell)liti, : $ 9DEF4 <= GD4 9DEF4 17. HIB4 &
Def. : acute diffuse suppurative inflammation.
Aetiology : increase streptococcus haemolytics "ecause it is pyogenic & produce
hyaluronidase enyme 2 fi"rinolycin enyme.
(athogene,i, : pathogenesis of pus 1 as "efore 3 F no one formation.
N@# : 1. site : loose ,.T 4x : or"it 2 axilla 2 scrotum.
!. 6iffuse area w` is congested , edematous , swollen , red , painful
& there is multiple s-in scars.
M@# : .ame as a"scess. $ ABC@ &
%ompli+ation, : %s a"scess except : chronicity
ulcer
)o sinus
7istula
A0,+e,, %ell)liti,
Def: %cute localied suppurative inflammation
ch` "y pus containing cavity.
%cute diffuse suppurative inflammation.
%a),e4 .taph. aureus. .treptococcus hemolyticus
(atho5
gene,i,4
1. +us formation
!. 8elease of co*agulase enyme localie
inflammation & divide it into ones1early
, late3.
;. +us is ch` "y :
a. thic- 1large amount of liLuefied
fi"rin3
". contain few 8(,s.
c. contain few sloughs
.ame
!. 8elease of hyaluronidase enyme &
fi"rinolysin causing spread of acute
inflam. 1no one formation3
;. +us is ch` "y :
a. thin 1 due to fi"rinolysin3
". contain much 8(,s.
c. contain much slough.
N@#4 1.,ardinal signs of acute inflam.
!.Nones:
as "efore
1..ite : CCCCCC. as "efore.
!.6iffuse areaCCCC as "efore.

&p*ead4 'ess common /ore common
II5A+)te non5 ,)pp)*ati<e inflammation
FF 8(,s: hemorrhagic inflammation
FF fluid exudate: serous?serofi"rinous?,atarrhal
FF necrosis: )ecrotiing*mem"ranous*%llergic
%ata**hal inflammation:
Def: /ild acute inflammation of > /./ characteried "y FF mucous secretion.
&ite,: /./ of 8.T or 0IT. > "est -nown example is > common cold #corya# ,atarrhal rhinitis.

N@# : /ucus mem"rane is :edematous , congested , swollen and red
& covered e` : 1
,t
serous fluid then mucoserous then mucus.
M@# :
1.4pithelium may "e degenerated , swollen , necrotiing or shedding.
!..u"*epithelium : /?4 of acute inflam. $ABC@ & as "efore.
Fate:
1& inflammation su"sides & regeneration occur.
!& !ry infection e pyogenic "acteria $exudate "ecomes muco*purulent&.
;& chronic inflammation metaplasia of surface epithelium & fi"rosis of
underlying tissue.
Be,t ;i,he,
Mem0*ano), (p,e)domem0*ano),) inflammation
Def: ,haracteried "y formation of mem"rane formed of fi"rin, desLuamated epith
& inflam ,s.
%a),e: (acteria w have a low invasive capacity "ut grow on > surface of mucous mem"rane &
produce exotoxins as : *1. 6iphtheria !* .higella $causing "acillary dysentry&.
&ite : mucous mem"rane $/./&.
(athogene,i,4*"acteria stic- to > surface of $/./& releases potent exotoxin. superficial
necrosis & acute inflammation of underlying tissue. %s > exudate passes to > surface > fi"rinogen in
it clots & encloses > necrotic epithelium in fi"rin networ- to form > pseudomem"rane w contains
also "acteria, neutrophils & 8(,s. )eutrophils accumulate at junction of living & dead tissue.
their digestive enymes detach > pseudo mem"rane leaving a raw surface.
*Toxemia $as exotoxins are a"sor"ed in > (I. stream&.
N@# : mucuc mem"rane appear as patches w` are :* $ D i )
* multiple.
* varia"le.
* irregular.
* grayish yellow in color.
* firmly adherent to underlying tissue.
* slightly raised a"ove surface .
* if removed "y force , leave "leeding surface & reform rapidly again.
* later : spontaneously detached.
M@# 4
1.4pithelium : replaced "y pseudomem"rane w` contain :
* fi0*in net;o*? intangling e2in it, me,he, E ne+*oti+ ti,,)eBo*gani,m B inflam.+ell,F
* necrotic tissue.
* organism
* inflam. cells.
!..u"*epithelium : /?4 of acute inflam. $ as "efore &
Fate:1& 8e*epithelialiation !&'oss of mucosal glands & fi"rosis.
Be,t ;i,he,
&e*o), inflammation
Def: %cute inflammation characteried "y FF watery fluid exudate.
&ite:.-in as in herpes simplex & "urn where watery vesicles are seen.
&e*ofi0*ino), inflammation
Def: %cute inflammation characteried "y > formation of FF fluid exudate rich in fi"rinogen
,ause:It occurs e more severe injuries & greater vascular permea"ility allows > passage of
fi"rinogen molecules.
&ite: $1& inflammation in serous sacs $pleura, pericardium & peritoneum&.
$!&lung alveoli $lo"ar pneumonia&.
(athology :
N@#: $1&+arietal & visceral layers "ecome red, opaLue, rough & thic-ened.
$!&7ine gray granules # fi"rin are seen on "oth internal surfaces.
$;&.erous fluid collects in > cavity
$<&%ccording to proportion of serous fluid & fi"rin. If FF fi"rin deposition is
of dry type. If FF serous fluid collects in > sac,> wet type.
M@#4 $1&.erosa of > visceral & parietal layers are swollen or desLuamated "are
surfaces.
$!&fluid exudate rich in fi"rinogen from > "are surfaces changes to fi"rin
networ- on "oth > visceral & parietal layers entangling acute inflammatory ,s
$;& su"serosa shows hyperemia, edema & fi"rin networ- enclosing the
inflammatory ,s.
Fate4 repair "y organiation.
Hemo**hagi+ inflammation
Def: %cute inflammation characteried "y vascular damage hemorrhage
%a),e :.evere injuries sufficient to cause vascular damage.
%a),ati<e 0a+te*ia: .mall pox, meningococci, strept. hemolyticus &8ic-ettsia.
Ne+*otizing inflammation
Def: It is acute inflammation characteried "y extensive tissue necrosis e.g..
$1& :incents angina & cancrum oris in > mouth.
$!& Infective gangrene
Alle*gi+ inflammation:
% type of infam.l in w` inflammatory reaction results from antigen ?anti"ody reaction.
Be,t ;i,he,
%o)*,e of a+)te inflammation depend, on :
a& type of tissue inflamed
"& amount of tissue destroyed $w depends on > nature & severity of > irritant&.
Fate of a+)te inflammation
1- "e,ol)tion# complete restoration of tissues to $)&normal after acute inflammation.
conditions that favor resolution are::
a*/inimal or no cell death.
"*8apid removal of inflammatory exudate. e.g. 'o"ar pneumonia.
35 Healing 0y fi0*o,i,. %fter tissue destruction:
a*In tissues that can not regenerate.
"* a"undant fi"rin or necrosis
75 (*og*e,,ion to +h*oni+ inflammation
A5 ,p*ead death.
JKLMNNJ NNO(P$$PQNMN
Def: inflammatory process in w lymphocytes, plasma ,s & macrophages predominate F
formation of granulation tissue fi"rosis.
%a),e,: $1& follows acute inflammation or
$!& ,hronic de novo
ype, of +h. inflammation :
15non5,pe+ifi+ :
*6ifferent irritants can produce this reaction so > etiology canHt "e identified from >reaction.
* follows acute inflammation e.g. +h*oni+ a0,+e,,.
35,pe+ifi+ 9g*an)loma:
4ach irritant produces a specific inflammatory reaction & so etiology can "e identified from
reaction e.g. tu"erculosis, "ilhariasis.
'ene*al feat)*e, of +h*oni+ inflammation
1&> irritant is mild F prolonged action.
!& 5nset is gradual & duration is prolonged.
;& Initial tissue necrosis not mar-ed.
<& :ascular phenomenon less mar-ed than acute type. A*te*iole, ,ho;
thi+?ening = na**o;ing 0y p*olife*ation of G ,)0intimal %# #nda*te*iti,
o0lite*an,.(#AO) !
=& 7luid exudate is not mar-ed.
K& ,ellular exudate consists of:*
a5lympho+yte,: main cell of ch. inflammation, change to plasma cell & secrete
lympho-ine .
05pla,ma %,: produces anti"odies.
+5 ma+*ophage,: are phagocytic ,s widely distri"uted in tissues & Their functions are4
*phagocytosis of necrotic de"ris & "acteria & other irritants
* scavenger ,s in repair
*7ormation of epithelioid ,s & giant ,s
d5 giant %,: formed "y fusion of macrophages. It may "e:
i *'anghanHs giant cell type: when > nuclei are peripherally situated specially in
tu"erculous lesions.
ii* foreign "ody giant cell type: when > nuclei are placed centrally as 7.( reaction.
$O& %ssociated e repair.
PPPPPPPPPPPPPPPPPPPPPPPPPPPPPP
N.B4 "#$ %! &'()
M@# of +h*oni+ inflammation i, :
1. 4%5 : arterioles show thic-ness&CCCCCC ( a, a0o<e ) *+"
!. 7i"rosis.
;.,hronic inflammatory cells :
* lymphocytes :CCC.
* plasma cells :CCCC a, a0o<e @RF4 ST
* macrophage :CCC..
* giant cells , fi"rocytes :CC.
%h*oni+ non ,pe+ifi+ inflam.:*
/?4 : as a"ove.
%h*oni+ ,pe+ifi+ inflam. :*
/?4: as a"ove F specific features that we can recognie organism from it.
PPPPPPPPPPPPPPPPPPPPPPPPPPPPPP
'*an)loma,
Def : ,hronic specific inflammatory reaction in ;2 the hi,tio+yte, play a p*edominant
*ole. It ,ta*t, a, tiny g*an)le, ; f),e to fo*m t)mo*5li?e ma,, g*o,,ly.
ype, :
1. Infective granuloma: a*(acteria: e.g. tu"erculosis $T(&, leprosy & syphilis$Q&
"* :irus: lymphogranuloma inguinale
c* +arasites: e.g. "ilhariasis.$(&
d* 7ungi: %ctinomycosis.
!. )on infective granuloma:
a*%llergic granuloma: as 8heumatic fever, 8heumatoid arthritis
&crohnHs disease.
"*7oreign "ody granuloma: around foreign "odies as "eryllium, catgut, talc powder.
fo*eign 0ody giant %, a*e a p*ominent feat)*e.
c* 0ranulomas of un-nown cause: as sarcoidosis.
Mi+*o,+opi+ pi+t)*e :
$1) &pe+ifi+ to each irritant .> irritant may "e seen inside or outside phagocytic ,s.
$!& :ascular change may not "e apparent.
$;& /acrophages, epithelioid ,s & 7" giant ,s are > main ,s of a granuloma.
$<& 'ymphocytes & plasma ,s.
$=& 7i"rosis.
Be,t ;i,he,
B5"#(AI"
Def : replacement of damaged tissue "y a healthy one.
* occurs when "ody defense & treatment destroy the irritant.
* macrophages then clean the area $scavenger ,s&
ype, of *epai* 4
1.Healing 9 *epai*
3."egene*ation : replacement of damaged tissue "y same -ind of tissue.
7.Fi0*o,i, : replacement of damaged tissue "y fi"rous tissue.
A.O*ganization : replacement of non*living tissue "y fi"rous tissue.
4x: throm"us 1non*living tissue3 can "e transformed to "e fi"rous tissue 1 living 3.
H."e,ol)tion : type of repair w` occur e`out cell proliferation.
* occur only "y a"sorption if no necrosis.
15 "#'#N#"AION
Def 4 replacement of the damaged tissue "y a healthy tissue of the same -ind.
.o regeneration depend on :*
1.4xtent of damage only in sta"le cells:
a. if small : regeneration.
". if large : fi"rosis.
!..tage of framewor-:
a. if injury to parenchyma only : regeneration.
". if injury to parenchyma F stroma 1framewor-3 : fi"rosis.
;.Type of cells:
La0ile +ell, &ta0le (e*manent
Def. ,ells in continuous
state of proliferation
,ells e` limited capacity of
proliferation
,ells e` no a"ility to
proliferate
#/. 1. cells of epithelial
surface
!."one marrow cells
;.lymphoid tissue
1.parenchematous cells of all
gland
!.mesenchymal cells as osteo"last
& chondro"last
1.nerve cells
!.s-eletal ms. cells
"epai* (y regeneration *if small damage:regeneration
*if large damage : fi"rosis
(y fi"rosis 1 gliosis
only in nerve cells 3
#6AM(L#&:
I5"egene*ation of ,?in:
4pidermal ,s $la"ile ,s& regeneration
6ermis fi"rosis e a"sent s-in appendages $hair follicles, se"aceous & sweet
glands.&
II5 "egene*ation of li<e* %,:
1 * mild damage F intact fi"rous framewor- e.g. mild viral hepatitisregeneration
! * severe damage F destroyed fi"rous framewor- e.g. severe viral
hepatitis, cirrhosis $loss of > $)& liver architecture&.
Be,t ;i,he,
III5 "epai* of ?idney,4
1*tu"ulear damage: a* intact ".m as in tu"ular necrosis 8egeneration
"*destroyed ".m as in infarction 7i"rosis.
!* glomerular damage 7i"rosis.
I-5 "epai* of m),+le,: s-eletal, cardiac & smooth muscles fi"rosis.
-5"epai* of 0one f*a+t)*e45
1. for normal "ony union : ! "ony end must "e fixed against each other.
!. at site of fracture : there is Ege, necrotic tissue w` are cleaned "y astrocytes ,macrophage.

;.provisional # procallus formation :
Def. : modified type of granulation tissue formed during process of "one healing.
Fo*med 0y : invasion of heamatoma at site of fracture "y capillaries , fi"ro"last ,
osteo"last w` lay down osteoid tissue.
ype,: 1. 4xternal callus : w` encircle "ro-en end from outside.
!. Internal callus : w` encircle "ro-en end from inside.
;. Intermediate callus: w` directly unite "ro-en ends.
<.permanent "one formation 1 final remodeling 3 :
* external & internal callus : removed "y osteoclast.
* intermediate callus undergo ossification , calcification : form lamellar "one
* "one marrow : regenerate.
* final remodeling is completed in a"out one year.
=.complication # anomalies 4
* non union due to soft tissue interposition $ & "ony ends. 4x:muscle
* malunion due to imperfect reduction.
* delayed union due to : infection 2 ischemia 2 old age.
* fi"rous union due to poor immo"iliation of "ones.
:I* 8epair in nervous system:
A) In %N& :
1. nerve cells repair "y gliosis as it is permanent cells.
!.me+hani,m: destruction of any part of neuron then astrocytes proliferate &
produce gliosis.
B) In (N&4
1. ,utting of nerve : ! types of degeneration affect "oth segments of cut nerve:*
A5Ni,,el 9 *et*og*ade degene*ation4
* nucleus: eccentric , small , dar- stained.
* nissel granules : disappear.
* cells : a"sor" E!5 .o "ecome swollen.
* dendrites : disappear.
B5Ialla*ian degene*ation :
* axon : fragmented.
* myelin sheath : "rea- down to myelin droplet.
P(oth are a"sor"ed "y macrophageP
Be,t ;i,he,
!.8egeneration # 8ecovering:*
* nucleus : central in position.
* nissel granules : regenerate.
* cells : normal sie.
* axon : grow from proximal segment in rate 1*; ml ? day.
* myelin sheath : reformed "y proliferation of schwan cells on "oth sides.
%ompli+ation of *epai* in (N& :,t)mp E t*a)mati+F ne)*oma:
Def. : 9hitish painful mass composed of nerve axons , fi"ers at cut end of nerve
due to non*aproximation of two end together.
35,ealin- .y fi.rosis/
'*an)lation ti,,)e: transitional tissue #repair tissue following acute inflammation or associates
chronic inflammation and followed "y fi"rosis =consist of capillaries and fi"ro"last.
* &t*)+t)*e (M@#)4it is formed of :
1*/any new capillaries lined "y swollen endothelial cells without a "asement mem"rane.
!*7i"ro"last cells appear "etween > capillaries.
;*The ground su"stance "etween the capillaries and around fi"ro"lasts shows
homogenous, pale pin- exudate
collagen fi"ers $type III& transforms to "undles $type I&.
/ixed acute and chronic inflammatory cells.
* Me+hani,m of fo*mation 9 pathogene,i,4
1R /acrophage clean the area.
!R ,apillary proliferation : in < steps:*
- "udding.
- .olid cords.
- ,analiation.
- 4sta"lishment of circulation
;R 7i"ro"last activation : fi"rocytes are activated to fi"ro"lasts w` migrate to area.
%ha*a+te*, (N@#)4
1* red granular & velvety. !*moist ;* fragile "leeds easily
<*8esistant to infection $contain fluid exudate w contains macrophages&.
=* high a"sorptive power $as it is vascular&
K*)ot sensitive $as it is devoid of nerves&
5 Fate4 end, in fo*mation of ,+a*(fi0*o), ti,,)e)45
1 *7i"ro"lasts produce > ground su"stance & 1= types of collagen fi"ers $I,II,III
etc.$ d.t transformation from one type to another&. > ,s & fi"er lie in all directions.
!* ,ollagen compresses & o"literate > capillaries.
;* 7i"ro"lasts contract $termed myofi"ro"lasts as they develop actin filaments in
their cytoplasm. so > lesion gets smaller.
<* 7i"ro"lasts change to fi"rocytes.
=* 7i"rocytes & collagen fi"ers are remodeled.
K* 7inally a<a,+)la* fi0*o), ti,,)e (a ,+a*& is produced.
Be,t ;i,he,
Healing of ;o)nd, . ( #/ample of fi0*o,i, )
1*y )nion91
,t
inten,ion 3*y )nion
O++)* in .urgical wound ch` "y :*
* clean.
* minimal tissue loss.
* edge are
approximated together
* haematoma is minimal
Infected wound ch` "y :*
* infected.
* excess tissue loss.
* gapping edge.
* haematoma is mar-ed.
Inflam. "/. /inimal 4xcessive
Fl)id e/)date, /inimal 4xcessive
'*an)lation ti,,)e /inimal 4xcessive
i,,)e de,t*)+tion /inimal 4xcessive
Me+hani,m of *epai* 4pidermis cover 1
st
. 0ranulation tissue cover 1
st
.
Io)nd +ont*a+tion 'es mar-ed /ore mar-ed
ime +on,)med .hort +rolonged
&+a* left Thin , linear Thic- , irregular
%ompli+ation 8are /ore common
Healing of ;o)nd
1R Eealing "y primary union # 1
st
intension:*
* type of ;o)nd : clean non*gapping wound.
* me+hani,m :
6ay 1 : ga" is filled e` clotted "lood 2 covered "y sca" of dry clotted "lood
on surface.
6ay ! : * at "oth edges : epidermal regeneration occur e` formation of "asement
mem"rane & pass across "lood clot.
* neutrophil invade wound ga".
6ay ; : macrophage replace neutrophils & start phagocytosis.
6ay <,= : * granulation tissue fill ga".
* collagen fi"rils start to appear.
!
nd
wee- : * collagen increase accompany "y capillaries disappearance.
* sca" separate.
<
th
wee- : mature scar formed of regenerated epidermis , lost s-in appendage e` dense collagen
"undles in dermis.
!R Eealing "y !ry union # !ry intension :
5 type of ;o)nd :infected ga""ing wound.
5 me+hani,m :
similar to mechanism of 1ry union except differ in following :*
a. excess necrotic tissue ,inflam. ,exudates that must "e removed so ta-ing long period.
". epidermal regeneration occur "ut don`t cover ga" except after removal of
necrotic tissue & filling ga" "y granulation tissue.
c. large 0.T 1 granulation tissue 3 : so "ig scar is formed.
d. ;o)nd +ont*a+tion i, maJo* diffe*en+e done 0y myofi0*o0la,t,.
%ompli+ation of ;o)nd healing :
1* /ore common e` !ry union.
!*
,osmotic deformities : due to excess scarring .
7unctional trou"les : due to contraction of scar around joints.
Geloid : disscused later
.Luamous cell carcinoma may develop 0)t *a*ely.
4pidermal cyst # implantation cyst:
,yst filled e` -eratin due to proliferation of epidermal cells that may "e
trapped e`in depth of wound during epithelial regeneration.
,hronic ulcer , fistula , sinus : due to improper healing caused "y either :*
- persistent infection that destroy 0.T
- excess deposition of collagenat edge of wound e`out filling wound e` enough 0.T
0- ,ealin- .y or-ani1ation
Def : replacement of non*living tissue "y fi"rous tissue.
#/: throm"us 1non*living tissue3 can "e transformed to "e fi"rous tissue 1 living 3.
5 Healing of ,e*o5fi0*ino), inflammation of a ,e*o), ,a+4
1 * serous component of > inflammatory exudate is a"sor"ed.
! * fi"rin & cellular exudate change to a structurless mass removed "y
macrophages.
;* 0ranulation tissue arises from > su"serosal layer & covers "oth surfaces.
< * serosal ,s at > edges of> "are area proliferate & cover > granulating surface. 'ater on >
granulation tissue matures to fi"rous tissue.
#ffe+t,: according to extent of fi"rosis :*
F $l& 7ormation of white patch in serous mem"rane.
FF $!& (and adhesions $ & > two layers of > serous mem"rane.
FFF$;& ,omplete adhesion $ & > two layers of > serous mem"rane.
2/ 3iscuss serofi.rinous inflam4 5 ho6 can it heal K
An,;e* : as "efore a, a0o<e L me+hani,m of fo*mation of '. 789
Be,t ;i,he,
%OM(LI%AION& OF "#(AI"4
A5 oo le,, +ell)la* p*olife*ation 4
1*ulcer !*sinus ;*fistula <* stretching of a wea- scar incisional hernia.
6ef:
B5oo m)+h +ell)la* p*olife*ation = fi0*o,i, :
1. FFF granulation tissue protrudes a"ove > level of adjacent s-in & "loc- epitheliation.
!. FFF scaring ?eloid4 more common in young )egroes
%a),e: hereditary.
im"alance $ &collagen synthesis & destruction "y collagenase.
N@#: firm raised scar e claw* li-e processes.
M#: 6ense hyalinied collagen "undles parallel to > surface.
(*ogno,i,4 a* .preads progressively & then stop.
"* may recur after removal.

;* fi"rosis $according to > site&
a*scar in > s-in disfiguring
"* scar in tu"ular structure stricture of "owel, ureter ....etc.
c*scarring of heart valves stenosis or incompetence.
d*scarring of arterial wall aneurysm
e*fi"rosis in > liver may cirrhosis.
f*fi"rous adhesion in peritoneum
g*fi"rous an-ylosis of joints.
h*cere"ral scar cere"ral irritation & epilepsy.
< * painful .car as in stump neuroma.
=* epithelium may dip down into > underlying tissue forming implantation dermoid
K*sLuamous cell carcinoma rarely develops in a scar.
FA%O"& IM(AI"IN' (INHIBIIN') "#(AI" :
A5 Lo+al fa+to*,4
1 * infection !* foreign "ody ;* ischemia <*severe damage $FF necrosis&
B5 'ene*al (,y,temi+) fa+to*,4
15Age4 repair is more rapid & adeLuate in young age.
!5N)t*ition
a* ** protein particularly sulfur containing %% as methionin needed for collagen
synthesis ** repair.
"* **vitamin: i*vit , deficiency defective formation of collagen & "one
ii*vit 6 deficiency failure of calcification of "one
c* **metals: 1*inc deficiency : necessary for collagen synthesis.
!*,aFF deficiency: reLuired for ,T & "one
75Ho*mone,4 e.g. cortisol ** repair.
A5&y,temi+ di,ea,e: e.g. dia"etes mellitus FFsuscepti"ility to infectiondelay repair.
H5(hy,i+al agent,: e.g. ioniing radiation ** repair.
85%hemi+al, = d*)g, e.g. cytotoxic drugs ** repair.
Be,t ;i,he,
%ont*ol of *epai*45
15 %onta+t inhi0ition: direct contact $ & similar ,s suppress "oth division & motility.
In wounds d.t a"sence of contact inhi"ition, ,s can migrate to cover > wound
surface.
35 %hemi+al mediato*,: ,ell growth is controlled "y growth stimulation & inhi"ition.
a*,halones $Inhi"iting factors&: formed "y living ,s & ** mitosis in > neigh"oring
,s of > same type.
5i,,)e de,t*)+tion la+? of +halone, lo+allyB ,o adJa+ent li<ing %, +an p*olife*ate.
"*Trephones $0rowth factors&: stimulate mitosis of> dividing ,s. they contain:*
i* 4pidermal growth factor $407&: FF mitosis in epithelial ,s & fi"ro"lasts.
ii* +latelet*derived growth factor $+607&: FF mitosis in fi"ro"lasts & smooth ms.
iii* 7i"ro"last growth factor $707&: FF mitosis in fi"ro"last &FF vasculariation
$angiogenesis&.
iv* Transforming growth factor* a $T07*a&* FF mitosis in epithelial ,s.
v * T07*( & Tumor necrosis factor $T)7&FF collagen synthesis.
75%ollagen ,ynthe,i, = de,t*)+tion: net collagen accumulation depends on "oth
collagen synthesis $"y growth factors& & degradation $"y collagenases&.
A5 #/t*a+ell)la* mat*i/ p*otein,: consists of structural proteins F adhesive proteins.
* ,ollagen: # structural protein, forming most components of "asement
mem"rane.
* 7i"ronectin: # adhesive protein, w "inds > cell mem"rane e other proteins as
collagen & fi"rin. It is important in cell attachment & movement of ,s.
Be,t ;i,he,